injuries of ureter, congenital anomalies of ureter, renal calculi, retrocaval ureter

1. DR.A.S.SHIVA SARAVANAN,B.H.M.S.,M.D(HOM)
ASSISTANT PROFESSOR
DEPARTMENT OF SURGERY
VMHMC
SALEM
DISEASES OF EXCRETOY
SYSTEM

2. HAEMATURIA
Types
 Gross (visible to unaided eye).
 Microscopic (>5 RBC’s / HPF).
 Early (initial) haematuria:
 Urethral origin, distal to external sphincter.
Terminal haematuria:
 Bladder neck or prostrate orgin.
Diffuse (total) haematuria:
 Source is in the bladder or upper urinary tract.
False haematuria:
 Discolouration of urine from pigments such as food colouring and
myoglobin.
Silent haematuria is due to tumors of kidney or bladder
unless proved otherwise.
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3. CAUSES
Renal injury
Urinary stones
Wilm’s tumor
Tuberculosis
Renal cell carcinoma
Cysititis
Bladder tumour
Urinary bilharziasis
BPH, carcinoma prostate
Renal infarct
Glomerulonephritis
Blood dyscrasias 2/10/2017
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4. INVESTIGATION
Urine culture and sensitivity (urine test for haematuria –
Benzidine test).
Ultrasound to look for the stone, tumor in the urinary
tract.
Cystourethroscopy to look for bladder or urethral
pathology.
IVU look for function of the kidneys.
Urinary cytology for diagnosing urothelial malignancy.
Bleeding time; clotting time; prothrombin time; platelet
count.
CT abdomen.
Renal function tests – blood urea, serum creatinine.
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5. MANAGEMENT
Causes should be identified and treated.
Blood transfusion.
Antibiotics.
Nephro – ureterectomy for RBC; removal of stone from
kidney, ureter, urinary bladder.
Treatment of bladder tumour by cystoscopic resection;
intravesical chemotheraphy using BCG; radiotheraphy;
systemic chemotherapy.
Treatment of medical causes like glomerulonephritis.
Correction of BPH.
Correction of bleeding diathesis.
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6. HORSESHOE KIDNEY
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7. It is a developmental anomaly where there is failure of
complete ascent of kidneys with the fusion of lower or
upper poles.
It is due to fusion of subdivisions of mesonephric duct,
when the embryo is as early as 30-40 days old.
This condition is common in males.
Fusion of lower pole is common (rarely upper poles).
Commonest site is in front of the 4th
lumbar vertebrae.
The part in front of the vertebrae is called as isthumus.
It has blood supply which freely communicates one
kidney to other.
Isthumus usually lies in front of aorta.
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8. CLINICAL FEATURES
Presents as a fixed, nonmobile, firm mass in the
midline at the level of 4th
lumbar vertebra which is
resonant on percussion.
It is more prone for infection, stone formation,
hydronephrosis, tuberculosis.
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9. Diagnosis
IUV – medialisation of lower calyces and curving of
ureter like a ’flower vase’.
U/S abdomen.
Urine analysis, blood urea and serum creatinine are
supportive investigations.
CT abdomen.
Treatment
Whatever the complications occurs in horseshoe kidney,
it is treated accordingly. 2/10/2017
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10. CYSTIC DISEASES OF THE KIDNEY
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11. Kidney cyst Types
Genetic:
Adult polycystic kidney disease (Autosomal dominant)
Infantile polycystic kidney disease (Autosomal
recessive)
Nongenetic – Simple cyst, multicystic kidney,
medullary sponge kidney.
Acquired renal cystic kidney may develop in
patient on long term dialysis. 2/10/2017
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12. POLYCYSTIC KIDNEY DISEASE (PCKD)
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13. Adult PCKD is inherited as autosomal dominant disease. It is
common in females.
It is bilateral and presents in third decade. One side presents
little earlier than other side.
Aassociations
Polycystic disease of liver (18%), pancreas and lung.
Berry aneurysm in the circle of willis.
Cyst formation occurs at the junction of the distal tubule and
the collecting duct.
Grossly it contains multiple cysts with a clear or brownish
fluid (due to haemorrhage). 2/10/2017
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14. CLINICAL FEATURES
Bilateral palpable renal mass
Loin pain
Haematuria
Infection
Hypertension, uraemia.
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15. Differential Diagnosis
Renal cell carcinoma
Hydronephrosis
Solitary renal cyst
Investigations
U/S confirms the presence of cysts.
IUV – Spider leg pattern with an elongated compressed
renal pelvis, narrowed and stretched calyces.
Blood urea and serum creatinine to rule out renal failure.
Urine shows low specific gravity.
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16. TREATMENT
Wait and watch policy.
If one of the cysts overdistends causing pain, haemorrhage,
infection, then surgical intervention is required.
Rovsing operation – The kidney is exposed. The cyst is
opened. The fluid is evacuated. The cut edge is
marsupialised.
Presently U/S guided aspiration is done as a simpler
approach.
Laproscopic / retro peritoneoscopic aspiration / deroofing
of the renal cyst.
Once renal failure sets in, in then initial haemodialysis
followed by bilateral nephrectomy, is done and later renal
transplantation should be planned for.
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17. SOLITARY RENAL CYST
Solitary renal cyst is never congenital.
It is due to an earlier trauma or infection resulting in
blockage of tubule, leading to cyst formation.
It is usually unilateral, presents as a renal mass
which is smooth, often if infected or haemorrhagic.
Investigation
U/S and IVU confirms the diagnosis.
CT scan positive.
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18. TREATMENT
Kidney is exposed. The cyst is aspirated and a
portion of the cyst wall is removed
( Kirwin’s operation) and cavity is filled with
perinephric fat.
Occasionally if the cyst is in one of the pole, partial
nephrectomy is done.
Laparoscopic approach.
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19. RETROCAVAL URETER
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20. RETROCAVAL URETER
It is due to developmental defect of IVC, as a result
of which right ureter passes behind the IVC, causing
right sided hydronephrosis with upper third
hydroureter.
IVU shows hydronephrosis with ‘reverse J sing’.
Treatment: Anderson Hynes’ operation
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21. URETEROCELE
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22. URETEROCELE
It is a cystic enlargement of the intramural portion of
ureter due to congenital atresia of the ureteric
orifice. Its wall contains mucous membrane only.
It is common in females, often bilateral (10%).
Complication
Stone formation
Recurrent infection
Hydronephrosis
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23. INVESTIGATION
IVU-Shows Adder-head appearance or cobra head
appearance.
Cystoscopy-Shows translucent cyst which is thin
walled surrounding the ureteric orifice.
Treatment
Cystoscopic ureteric meatotomy with the removal of
cyst wall.
In addition to that co-existing complications should
be treated.
Often ureteric re-implantation is needed.
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24. INJURIES TO KIDNEY
Commonly it is due to a blunt injury.
Often it is associated with other abdominal injuries
of liver, spleen, bowel, mensentery, etc.
Per se renal injury is extraperitoneal.
TYPE OF RENAL INJURY
Small subcapsular
Large subcapsular
Cortical laceration
Laceration with perinephric haematoma.
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25. Medullary laceration with bleeding into the renal.
Corticomedullary complete rupture.
Hilar injury (most dangerous).
Grading Of Renal Injury
Subcapsular non-expanding haematoma without
parenchymal lanceration
Cortical laceration < 1 cm of parenchymal depth, no
extravasation; perirenal haematoma
Cortical lacertion > 1 cm depth; no urine
extravasation
Parenchymal laceration extending through cortex
and medulla with collecting system; with
extravasation of urine
Renal pedicle avulsion; shattered kidney
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26. CLINICAL FEATURES
Features of shock.
Haematuria-may be mild to profuse depending on
the type of injury.
Clot colic.
Bruising, swelling and tenderness in the loin.
Paralytic ileus with abdominal distension occurs due
to retroperitoneal haematoma implicating
splanchnic nerves.
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27. COMPLICATIONS
Clot retention in the bladder and may go for renal
failure
Pararenal pseudo hydronephrosis
Infection
Perinephric abscess
Aneurysm of the renal artery
Renal failure
Hypertension occurs 3 months later
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28. INVESTIGATIONS
IVU(high dose)-It is the investigation of choice. Here
function of not only the injured kidney but also of the
contralateral kidney can be soon. It is observed that often
opposite renal artery undergoes a reflex spasm, temporarily
ceasing the function of the contralateral kidney.
U/S abdomen-Done to see the type of injury, amount of
haematoma and other associated at regular intervals to see
the progress (at 12-24 hourly).
Blood urea and serum creatinine should be repeated at
regular intervals.
Blood grouping and cross-matching for blood transfusion.
Emergency CT scan is very useful.
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29. TREATMENT
Initially always conservation:
Catheterise and watch the urine colour and output.
Blood transfusion.
Sedation observation with regular monitoring of the
pulse, BP, temperature, U/S follow-up daily.
75% of patients respond to conservative mana-
gement.
While treating conservatively, regular monitoring of
blood urea and serum creatinine is a must.
If the patient goes in for 6-8 weeks. Meanwhile,
other kidney starts functioning again and patient
recovers without any further problem.
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30. Indications for surgical intervention:
 When there are signs of progressive blood loss with the
condition of the patient deteriorating.
 Formation of progressive perinephric haematoma.
 When there are associated other injuries.
 Hilar injury.
Surgery Options:
Gentle suturing of the laceration. Often kidney is
friable, this is not possible.
Then nephrostomy is in the poles partial
nephrectomy is done.
In hilar injury and severe laceration, nephrectomy
is the only choice.
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31. RENAL CALCULI
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32. RENAL CALCULI
It is more common in
males;
90% are radiopaque
(gallstones are more
common in females; 90%
are radioluscent).
AETIOLOGY
Diet: Vitamin A
deficiency – it causes
desquamation of
epithelium which acts as
a nidus for stone
formation. 2/10/2017
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33. Climate: In hot climate urinary solutes will increase
with decrease in colloids, which leads to chelation of
solute with calcium forming a nidus for stone.
Citrate level in urine (300-900 mg/ 24 hours)
maintains the calcium phosphate and carbonate in
soluble state and any decrease in citrate level in urine
causes stone formation.
Infection in kidney: Urea splitting organisms
commonly cause stone formation.
Prolonged immobilization causes decalcification of bones
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34. Hyperparathyroidism causes hypercalciuria causing
multiple bilateral stones or often bilateral
nephrocalcinosis.
Hyperoxaluria, as a result of altered glycine metabolism.
Cystiniuria.
Stasis due to obstruction to urine flow.
Medullary sponge kidney.
Randall’s plaque theory is erosion and deposition of
urinary salts as Randall’s plaque at the apex of renal
papillae. 2/10/2017
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35. Carr’s postulates states that minute concentrations called
as microliths normally develop in the subendothelial part
of the tubule which will be carried away as particles by
renal lymphatic network vessels. If these lymphatics are
blocked, microliths enlarge and acts as nidus for stone
formation.
Others: sarcoidosis, myelomatosis, gout, idiopathic
hypercalciuria, hypervitaminosis D, neoplasms on
treatment, hypomagnesuria.
Renal tubular acidosis: Commonly causes calcium
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36. Stages of stone formation
 Supersaturation
 Nucleus formation
 Crystillisation
 Aggregation
 Matrix formation
 Stone
Epitaxy:
Growth of one type of stone on another type.
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37. RENAL CALCULI-TYPES
Oxalate stones (75%) also called as mulberry stone as it is
brown in colour, with sharp projections.
 It is invariably calcium oxalate stone, shows envelope
crystals in urine.
Phosphates stones (10-15%): it is either calcium
phosphate or calcium, magnesium, ammonium
phosphate stone usually occurring in an infected urine.
 It is smooth and white occurring in an infected urine. It
is smooth and white in colour.
In an alkaline urine it enlarges rapidly, filling renal
calyces taking their shape called as staghorn calculus. It
is radiopaque and attains a large size. 2/10/2017
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38. 2/10/2017
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39. 2/10/2017
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40. Uric acid stones are smooth, hard, yellowish, multiple
and radioluscent. They are seen in gout,
hyperuricosuria, altered purine metabolism.
Urate stones.
Cystine stones occur in cystinuria where there is
defective absorbtion of cystine from the renal tubules. It
is seen in young girls, occurs only in acidic urine.
It is multiple, soft, yellow in colour changes to greenish
hue on exposure. It attains large size.
It is radiopaque because it contains sulphur. 2/10/2017
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41. Xanthine stones are very rare, smooth, brick red in
colour, due to altered xanthine metabolism. Here
there is deficiency in xanthine oxidase enzyme.
Indigo stones: very rare. Blue in colour.
Struvite stone: it is compound of magnesium,
ammonium phosphate mixed with carbonate. It
occurs in presence of ammonia and urea splitting
organisms in urine, eg. Proteus; Klebsiella.
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42. CLINICAL FEATURES
Pain – renal pain is located over renal angle,
hypochondrium and lumbar region.
 Often severe radiating to groin and testis in males, with
vomiting due to pylorospasm. Pain worsens on movements.
Haematuria is common, Pyuria, Fever.
Tenderness in renal angle, with often a mass in the loin due
to hydronephrosis which moves with respiration and is
bimanually palpable, ballotable, smooth, soft.
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43. As urinary tract infection.
Incidental finding.
Often hypertension
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44. INVESTIGATIONS
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45. Blood: ESR, serum calcium, phosphate, creatinine,
blood urea, uric acid, PTH level.
Urine: Calcium, urate, cystine if suspected only pH,
specific gravity.
Plain X-ray, KUB: to see kidney shadow, stones
(90% - radiopaque).
IVU to see renal functions and HN.
RGP if required.
U/S abdomen – can detect even radioluscent stones
and gives information about the changes in renal
parenchyma.
Urine analysis and C/S to identify bacteria.
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46. SURGICAL TREATMENT
PCNL (Percutaneous Nephrolithotomy)
Indications:
Stones more than 2.5cm in size.
Multiple stones
Stones not responding for ESWL
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47. Procedure:
 Under the guidance of C-Arm or U/S, needle puncture is made in
the loin percutaneously. Through kidney, calyx and pelvis are
approached. Guidewire is passed. Graduated dilators are passed
and so track is widened. Then through that, a nephroscope is
passed. After fragmentation, stone is removed using different
methods.
COMPLICATIONS OF PCNL
Haemorrhage
Perforation of collecting duct
Injury of collecting duct 2/10/2017
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48. ESWL (Extracorporeal Shock Wave Lithotripsy)
Piezo-Ceramic or Electromagnetic shock waves are
passed to the stone through water bath or water n
which acts as a media. Shock are produced at 2/sec,
1000-4000 shocks are required for each stone.
Dornier Lithotripter is used for fragmenting stones.
Stone is located and observed through fluoroscope
(C-ARM) or ultrasound. Shock waves are triggered to
create compressive waves over the stone, to fragment
it. These fragments are flushed out later.
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49. SURGERIES
Pyelolithotomy.
Suitable for stones in extra renal pelvis.
By loin incision, kidney is approached.
Renal pelvis is opened, the stone is removed and
pelvis is closed. A drain is placed and wound is
closed
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50. Extended pyelolithotomy:
 In case of intrarenal pelvis, incision is done on the hilum between the
pelvis and kidney over the renal sinus, dissection is carried out so as
to remove the stones from pelvis as well as calyces.
Nephrolithotomy:
 By placing incision just behind the most convex surface, stone is
removed.
Nephropyelolithoyomy:
 by making incisions both over the kidney and pelvis, stones / stones
are removed. It is often done in staghorn calculus.
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51. Partial nephrectomy: done when there are multiple
stones occupying a pole, usually lower pole of the
kidney or when there is damage to the calyx, if not
removed may encourage further stone formation.
Bench surgery: kidney is removed out temporarily,
cooled by ice packs or inosine or liquid nitrogen.
Stones are searched and removed completely. Later
kidney is replaced in right iliac fossa.
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52. Anatrophic pyelolithotomy: after exposing the
kidney, it is cooled with ice packs for 20 minutes and
posterior branch of the renal artery is clamped
temporarily using bull-dog clamp.
 The most avasular plane behind the Brodel’s line is
thus visualized properly. Kidney is opened trough
this line and stone/stones are removed
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